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Menopause, hormone treatment and urinaryincontinence at midlife.
Guillaume Legendre, Virginie Ringa, Arnaud Fauconnier, Xavier Fritel
To cite this version:Guillaume Legendre, Virginie Ringa, Arnaud Fauconnier, Xavier Fritel. Menopause, hormonetreatment and urinary incontinence at midlife.. Maturitas, Elsevier, 2013, 74 (1), pp.26-30.�10.1016/j.maturitas.2012.10.005�. �hal-00779771�
1
Title 1
Menopause, Hormone Treatment and Urinary Incontinence at Midlife 2
3
Authors 4
Guillaume Legendre 1,2 5
Virginie Ringa 1 6
Arnaud Fauconnier 3,4 7
Xavier Fritel 5,6 8
9
Institutions 10
1. INSERM UMRS 1018, CESP Centre for Research in Epidemiology and Population 11
Health, U1018, Gender, Sexual and Reproductive Health Team, Paris-Sud University, 12
Villejuif, and Institut National des Etudes Démographiques, Paris, France 13
2. Bicêtre University Hospital, Assistance Publique-Hôpitaux de Paris, Le Kremlin Bicêtre, 14
France. 15
3. Research unit EA 7285, Versailles-St-Quentin University, Montigny-le-Bretonneux, 16
France. 17
4. Poissy-Saint-Germain-en-Laye Hospital, Poissy, France 18
5. INSERM CIC0802, Poitiers University Hospital, Poitiers University, France. 19
6. INSERM UMR S953, Epidemiological Research on Perinatal Health and Women and 20
Children Health, Paris 6 University, Paris, France 21
22
Correspondence 23
Prof Xavier Fritel 24
Service de Gynécologie-Obstétrique et Médecine de la Reproduction, 25
CHU de Poitiers, 2 rue de la Milétrie, F-86000 Poitiers, France. 26
Phone: +33 549 443 360; fax: +33 549 443 910 27
29
2
Abstract 30
Whether there is any association between urinary incontinence and menopause is the subject 31
of debate, partly due to the fact it is difficult to tell the difference between the effects of 32
menopause and those of ageing. For some time it was hoped that hormonal treatment for 33
menopause would be beneficial for urinary incontinence because there are hormonal receptors 34
in the urinary tract. The goal of this survey of current knowledge on the subject is to explore 35
thoroughly the relationship between menopause and urinary incontinence . 36
Our study is based on a review of the literature dealing with the epidemiology of urinary 37
incontinence in women aged between 45 and 60, and the effects of hormonal treatment with 38
respect to the symptoms of involuntary loss of urine. 39
Analysis of the epidemiological data drawn from large cohorts shows that on the one hand, 40
the menopause has little if any impact on the risk of urinary incontinence, and on the other 41
hand that the effects of œstrogen medication on urinary incontinence vary according to how it 42
is administered and the type of incontinence. The effect of oral hormone treatments for 43
menopause is rather negative with respect to stress incontinence. Vaginal treatment appears to 44
be beneficial for overactive bladder symptoms. 45
46
Key-words: Urinary Incontinence, Stress Urinary Incontinence, Urge Incontinence, 47
Overactive bladder, Menopause, Hormone therapy, Œstrogen, Epidemiology. 48
49
No conflicts of interest to declare. 50
51
3
1. Introduction 52
The menopause is a universal physiological event related with the drop in ovarian hormone 53
secretions (œstrogens and progestin) that occurs as the stock of ovarian follicules is depleted. 54
Menopause is diagnosed when menstruation has stopped for 12 successive months, and the 55
average age at which it occurs is between 47 and 51 [1,2]. Its clinical expression varies very 56
considerably between socio-cultural groups and individuals [3]. These variations depend on 57
many factors, such as women's social status, their nutrition, life style (smoking) and weight, 58
not forgetting genetic factors [3]. It is difficult to draw the distinction between the effects of 59
menopause and those of ageing. In addition to the menopausal "syndrome" itself, which 60
mainly comprises vasomotor symptoms and vaginal dryness, urinary symptoms including 61
incontinence (UI) have been attributed to menopause. The hormonal dependence of the 62
genital tract tissues has been evoked in order to explain the appearance of these female low 63
urinary tract symptoms (FLUTS) at the menopause. Œstrogen receptors have been found not 64
only in the pelvic floor muscles but also in the uro-genital ligaments and detrusor muscle cells 65
along with the connective tissues and all the fascias that maintain a stable relationship 66
between the various organs [2]. 67
Urinary incontinence can be defined as "the complaint of any involuntary leakage of urine" 68
[4]. The standard classification gives three main types of UI: Stress Urinary Incontinence 69
(SUI), Urge Urinary Incontinence (UUI) and Mixed Urinary Incontinence (MUI). Stress 70
urinary incontinence is characterised by involuntary loss of urine without any previous feeling 71
of a need to void, which takes place on the occasion of a physical stress (cough, lifting 72
something heavy, or any other physical activity). Urge urinary incontinence (or urgent need to 73
void) is characterised by involuntary loss of urine preceded by an urgent and irresistible need 74
to void resulting in uncontrollable leakage of urine. Mixed urinary incontinence is the 75
association in variable proportions of SUI and UUI. 76
UI may be experienced simply as a nuisance or as a real handicap [5,6]. Women frequently 77
present the symptoms of UI, but the estimates for its prevalence in the general population vary 78
widely, from 8 to 30 %. This variability is due not only to the very heterogeneous nature of 79
the populations studied but also to the varying definitions of UI used in the studies. 80
Many different factors are associated with an increased risk of UI [7]. The main of these are 81
ageing, pregnancy, childbirth, past history of pelvic and perineal surgery, obesity, and chronic 82
pathologies (diabetes, cognitive problems, etc.). There is more debate about the roles of 83
menopause and hormone replacement therapy (HRT) [8,9]. As mentioned above, it is difficult 84
4
to differentiate between the role of ageing and that of the menopause, and equally to 85
differentiate the true role of menopause from that of treatments instigated at the time of 86
menopause, such as HRT. 87
The relationship postulated between UI and hormone deficiencies induced by menopause is 88
based mainly on "physiological" data, i.e. the existence of (œstrogen and progestin) hormonal 89
receptors in the epithelial tissues of bladder, urethra and trigone and also in the vagina, 90
uterosacral ligaments, levator ani and puborectal muscles [10]. The other argument supporting 91
this relation is clinical observation of an increase in the prevalence of overactive bladder 92
(OAB) syndrome after the menopause. The lack of œstrogens could contribute in various 93
ways to other urinary symptoms that arise: œstrogens play a role in (i) the increase in 94
epithelial cellular trophicity in the vagina, urethra and bladder (ii) the increase in peri-urethral 95
vascularisation (an important factor for regulation of closing pressure), (iii) the increase in 96
maximum closing pressure and (iv) the increase in concentration and sensitivity of -97
adrenergic receptors with modification of the -adrenergic receptors/-adrenergic receptor 98
ratio in favour of the -adrenergic receptors [11-13]. Progestin receptors are also to be found 99
in the entire female genital tract, although in less constant fashion than œstrogen receptors. 100
Progestin appears to have a detrimental effect on continence, by reducing muscle tone of 101
bladder and urethra [10]. 102
The aim of our review is to analyse the data in the literature with respect to the relationship 103
between menopause and UI. We present the main epidemiological data dealing with the 104
relationship between prevalence, incidence and remission of UI, and the menopause. We then 105
try to supply answers to the two main questions raised by this relationship: What 106
consequences do hormonal changes at the menopause have on UI symptoms? What 107
consequences do hormonal treatments have on continence? 108
109
2. Methods: 110
A review of the literature was carried out by consulting the Medline database entries between 111
January 2000 and June 2012. Articles were selected by cross-referencing the following 112
keywords: "urinary incontinence, stress urinary incontinence, urge incontinence, overactive 113
bladder, menopause, œstrogen therapy". In this selection priority was given to meta-analyses, 114
literature reviews, randomised controlled trials and cohort studies. The level of evidence (LE) 115
5
scale proposed by the Oxford Centre for Evidence-Based Medicine (www.cebm.net) was used 116
to class the articles selected. 117
The terminology used complies with International Continence Society (ICS) and 118
International UroGynecological Association (IUGA) recommendations. 119
120
3. Results 121
3.1. Study selection 122
Among the 488 articles initially selected during the Medline search, 29 articles were finally 123
retained, including 3 meta-analyses, 4 literature reviews, 5 randomised controlled trials and 12 124
cohort studies. Figure 1 gives details on this selection of articles. 125
126
3.2. Prevalence or incidence of UI according to age 127
The prevalence of urinary incontinence is proportional to age. The distribution of the various 128
types of UI changes with age.Several articles report a peak in the prevalence of SUI at midlife 129
(LE3). The majority of cases before the age of 50 are SUI, but after that age it represents a 130
minority [14]. After 60 it is mixed UI that predominates. The prevalence of UI at the time of 131
menopause varies from 8 to 27 % depending on the population studied and the definition used 132
for UI [14-17] (LE2). 133
Only a few cohort studies specifically address the menopause period (45-60 years). Mac 134
Grother et al. report an annual incidence of UI of 8% in a population of 108 women aged 135
between 40 and 59 in the general population [16] (LE3). Two other cohorts of women under 136
the age of 60 found annual incidence rates at 4 and 5 % [15, 17] (LE3). In another cohort of 137
2860 femmes between 40 and 60, the authors report an annual incidence rate of 6% [18] 138
(LE3). A longitudinal study of a cohort of nurses aged 36 to 55 by Townsend et al. found an 139
annual incidence of 7% [19] (LE3). 140
There is considerable disparity between the cohort studies concerning the annual rate of 141
remission. On the one hand Hagglund [17], Samuelsson [20], and Townsend [19] report 142
annual remission rates for UI of 4, 6, and 7% respectively (LE3). On another hand other 143
authors report higher annual remission rates, at 25 to 29% [16, 18] (LE3). These results can be 144
explained in part by the definition of remission of UI depending on the studies: complete 145
disappearance or lessening of the severity of UI symptoms. 146
6
147
3.3. Prevalence or incidence of UI according to menopausal status 148
The American prospective cohort Study of Women’s Health Across the Nation (SWAN) 149
followed 1529 women, without any UI symptoms at inclusion, annually for 6 years. The 150
women were classed according to their hormonal status at the end of the study as follows: pre-151
menopause, early peri-menopause (irregular menses), late peri-menopause (3 to 11 months 152
amenorrhoea), and post-menopause (over 12 months amenorrhoea). The peri-menopause 153
period is associated with an increased risk of UI for all types of UI together (OR= 1.52 [95% 154
CI: 1.12Ŕ2.05] in late peri-menopause) but this association disappears post-menopause (0.88 155
[0.63-1.23]). Analysis by the type of UI shows that this association with the peri-menopause 156
above all concerns UUI (2.12 [1.26-3.56] in late peri-menopause) while the association is non 157
significant for SUI (1.24 [0.75-2.05] in late peri-menopause). Analysis of frequent UI alone 158
(at least one episode of UI a week) does not show any association with early peri-menopause 159
(0.99 [0.60-1.63]), late peri-menopause (1.14 [0.51-2.54]), or post-menopause (1.10 [0.46-160
2.64]) (LE2) [21]. In another study covering 2415 women from the SWAN cohort who were 161
incontinent (at least one episode of UI per month) at inclusion, Waetjen reports that the 162
worsening of UI symptoms observed after the menopause is not attributable to the menopause 163
itself [22] but to an increase in weight. The menopause appears to be associated with an 164
increase in weight and this would explain the increase in the prevalence of UI (LE2). 165
The study by Sherburn et al. of the Australian cohort of 1897 femmes, The Melbourne 166
Women’s Midlife Health Project, addressed the impact of the menopause on UI symptoms. 167
Simultaneous cross-sectional and longitudinal analysis of the data did not reveal any 168
statistical relationship between UI and menopause (LE3). In the longitudinal analysis of 438 169
women from the same cohort who were followed for 7 years the menopause was not 170
associated with any increase in the incidence of UI as a whole (LE3) [15]. 171
The results obtained by another longitudianl study, the National Survey of Health and 172
Development (NSHD) concerning 1211 women between 48 and 54 years of age did not find 173
any association between menopause and UUI (LE3). SUI alone was associated with the 174
hormonal status, since in this study the peri-menopause was associated with an increased 175
prevalence of urine leakage symptoms due to stress, as compared with the group of post-176
menopausal women (OR= 1, 39 [1, 4-1, 7]) (LE3). This study, in which it is not possible to 177
distinguish clearly between the effects of age and those of menopause because there is no 178
comparison of the incidence rates between the different groups, nevertheless appears to reveal 179
7
an effect of ageing independent of that of the menopause with respect to the occurrence of 180
UUI or SUI (LE3) [23]. 181
A large Chinese cross-sectional study of nearly 20 000 women aged 20 to 99 shows an 182
association between SUI and menopause (OR= 1, 26 [1, 04-1, 52]), even when age is taken 183
into account as a risk factor (LE4) [24]. 184
185
3.4. Prevalence or incidence of UI according to hormone levels 186
A recent cohort study looked at the effect of changes in œstrogen concentrations on urinary 187
symptoms during the transition to menopause. A big drop in œstrogen levels is associated in 188
significant fashion with an improvement in UI symptoms (LE2) [25]. Moreover, analysis of 189
the annual fluctuation in endogenous œstrogen levels during the menopausal period using the 190
data from SWAN did not find any association with the onset of UI or worsening of UI 191
symptoms (LE2) [26]. A Swedish cohort study of 6917 women aged between 50 and 59 even 192
found a positive association between a high œstradiol level and UI (LE2) [27]. 193
194
3.5. Prevalence or incidence of UI depending on menopause hormonal treatment 195
3.5.1. Data obtained from random studies of women treated for urinary symptoms 196
A meta-analysis based on eleven randomised studies of the effects of œstrogen (versus 197
placebo) on overactive bladder symptoms found a significant association between œstrogen 198
treatments and an improvement in the urinary symptoms: less pollakiuria and nocturia, fewer 199
episodes of UUI and urine leaks, improvement in the latence of the first urge to void and 200
increase in bladder capacity (LE1) [28]. However the effects vary according to the mode of 201
administration of the œstrogens. Local application (vaginal or intravesical) is associated in 202
significant fashion with an improvement in all the urinary symptoms (pollakiuria, nocturia, 203
UUI, bladder capacity). Systemic administration results in only partial improvement of these 204
symptoms, and statistically is associated only with a drop in the number of episodes of 205
incontinence and later perception of the first urge to void. 206
A review of the literature covering several randomised trials (comparisons between different 207
protocols for œstrogen treatment or versus placebo) confirms the advantage of vaginal 208
treatments in case of post-menopausal lower urinary tract symptoms, especially in the 209
presence of vaginal atrophy (LE2) [11]. The findings of recent studies of the effect of 210
8
œstrogens in association with anti-muscarini agents did not agree. A controlled study of 229 211
femmes presenting an overactive detrusor did not show any benefit for topical vaginal 212
œstrogen therapy associated with tolterodine versus tolterodine alone for overactive bladder 213
symptoms (LE2) [29]. Another randomised controlled trial in 80 women with overactive 214
bladder syndrome, also comparing the effect of topical vaginal œstrogen therapy associated 215
with tolterodine with that of tolterodine alone, found a significant improvement of objective 216
parameters and quality of life when œstrogens were associated with tolterodine (LE2) [30]. 217
Finally, a recent randomised trial comparing the efficiency of topical vaginal œstrogen 218
therapy with that of oxybutynin for the treatment of overactive bladder syndrome found that 219
the two products were similar in terms of efficiency (LE2) [31]. 220
A review of the literature covering eight controlled studies and 14 prospective non-controlled 221
studies concluded that œstrogen treatment is not efficient for SUI (LE2) [32]. 222
223
3.5.2. Data resulting from secondary analyses of randomised trials in the general 224
population 225
Among the post-menopausal women enrolled in the Womens’ Health Initiative study (WHI), 226
HRT significantly increased the incident risk at one year of all types of UI (SUI, UUI, MUI) 227
in women who were continent at the time they were included (LE2). This effect of HRT is 228
particularly distinct for SUI and less so if at all for UUI [33]. In women taking oral œstrogens 229
and progestin, the relative risk of de novo UI is 1.87 [1.61-2.18] for SUI, 1.15 [0.99-1.34] for 230
UUI and 1.49 [1.10-2.01] for MUI. The results are similar for women taking œstrogen alone: 231
2.15 [1.77-2.62], 1.32 [1.10-1.58], and 1.79 [1.26-2.53] respectively. In women who were 232
incontinent when included, HRT slightly increased the quantity lost (1.20 [1.06-1.36] when 233
treated using œstrogen and progestin and 1.59 [1.9-1.82] when treated with œstrogen alone), 234
and the frequency of leaks (1.36 [1.28-1.49] and 1.47 [1.35-1.61] respectively) [33]. 235
Steineauer et al. carried out a subsidiary analysis of the Heart Estrogen/Progestin 236
Replacement Study (a double-blind randomised study assessing the effect of HRT for 237
prevention of cardiovascular risks) concerning patients with no UI at inclusion [34]. A 238
significant relationship between HRT and the onset of both UUI and SUI was found during 239
the first four months of treatment. This detrimental effect of HRT persisted throughout the 4 240
years of the study, with a cumulated additional risk of 12% and 16 % respectively for UUI 241
and SUI compared with treatment by placebo (LE2). 242
9
The results of these studies were included and confirmed in the Cochrane Database [35] meta-243
analysis which covered a total of 19 313 incontinent women among whom 9417 were treated 244
by œstrogens, in 33 studies (16 of which addressed specifically SUI). There was no analysis 245
by type of UI. A worsening of UI symptoms was found when HRT was taken systemically 246
(RR= 1.32 [1.17-1.42]) (LE1). However, topical vaginal œstrogen therapy contributed 247
towards remission of UI by improving both the episodes of urge urinary incontinence (0.74 248
[0.64-086]) and pollakiuria (LE1). 249
250
3.5.3. Data obtained from cohort studies 251
The data of the Nurses’ Health Study addressing the impact of HRT on UI in a cohort of 252
nurses aged between 30 and 55 at the time of inclusion were analysed by Grodstein et al. [36]. 253
The occurrence of incident UI was associated in significant fashion with systemic hormone 254
therapy whatever the type of HRT and mode of administration: oral œstrogen (RR= 1.54 255
[1.44-1.65]), transdermal œstrogen (1.68 [1.41-2.00]), oral œstrogen and progestin (1.34 256
[1.24-1.44]) and transdermal œstrogen and progestin therapies (1.46 [1.16-1.84]) (LE3). The 257
overall risk of UI remained low however, with an annual incidence of 1.6%, and the effects of 258
HRT disappeared when treatment ceased. 259
A recent cohort study of post-menopausal women found an association between UI symptoms 260
and duration of œstrogen treatment. Prolonged oral œstrogen therapy (5 years or more) is 261
associated with a worsening of leakage symptoms (OR= 3.99 [1.21-13.1]) and also an 262
increase in the frequency of handicapping UI (3.97 [1.02-15.4]) [37] (LE3). 263
264
3.5.4. Data obtained from studies concerning intermediate markers 265
Certain older studies report that the use of oral œstrogens appears to increase the urethral 266
closing pressure and could thus improve SUI symptoms in 65 to 70% of women [38] (LE5). 267
Two randomised controlled trials concerning the oral route versus placebo to treat UI and 268
including 83 and 67 post-menopausal women were unable to demonstrate any effect of 269
œstrogens with respect to urodynamic parameters or urinary symptoms, whether in terms of 270
objective measurements (pad-test, cystometrography, prolifometry) or in terms of subjective 271
measurements (assessed by approved quality of life questionnaires) [39] (LE2). 272
273
10
3.5.5. Influence of hormonal treatment after surgery for SUI 274
Certain studies looked at the impact of œstrogen therapy when surgery is used for SUI. A 275
prospective randomised study comparing the effects of adjuvant topical vaginal œstradiol or 276
not for six months immediately after surgical correction of SUI using a sub-urethral tape 277
(TVT-O) in 183 post-menopausal patient, found that pollakiuria (2 vs. 11 %, p=0.02) and urge 278
urinary incontinence (3 vs. 12 %, p= 0.01) alone were improved by hormone therapy (LE2) 279
[40]. The objective parameters of the urodynamic tests remained unchanged in both groups 280
(LE2). In a randomised controlled trial Zullo et al. found exactly the same results with urge 281
urinary incontinence alone being improved by topical vaginal œstrogen therapy (LE2) [41]. 282
No study of the long-term advantages of œstrogen after installation of a sub-urethral tape was 283
found. 284
285
4. Discussion 286
The results of our review concerning the link between menopause and UI do not all agree, but 287
this overview shows that the menopause has little if any impact on the risk of UI in general, 288
when confounding factors such as age or changes in weight are taken into account. It appears 289
that SUI decreases after the menopause while UUI or mixed UI increase at this time. Oral 290
HRT has a rather detrimental effect on stress urinary incontinence, by doubling the risk of de 291
novo SUI. Concerning UUI, HRT has less of an effect, which is variable according to the 292
population in question and the type of treatment. Topical vaginal œstrogen therapy is the only 293
treatment that seems to have a really beneficial effect on urge urinary incontinence or 294
overactive bladder symptoms. 295
Most of these results are drawn from longitudinal analyses of large cohorts enabling a 296
distinction to be drawn between the effect of age and that of the menopause. Longitudinal 297
studies are the only way to examine the timing, and consequently any cause and effect 298
relationship between events. Cross-sectional studies cannot assess time-dependent variables 299
such as age, weight and menopausal status. Nevertheless, the large cohort studies included in 300
this review present several problems. For example, the definition of UI is not identical in all 301
the studies because follow-up of the cohorts often started prior to the harmonisation of the 302
terminologies proposed by ICS and IUGA. The frequency of UI as a "functional complaint" 303
depends on the tools used. Moreover, few of the studies draw a distinction between the 304
various types of UI (SUI, UUI, MUI), their frequency or their severity. Finally in this type of 305
11
cohort, the lack of any overall assessment of incontinence risk factors (because the studies 306
were not designed initially to study this problem specifically) can result in confounding 307
biases. 308
Part of the results of this review is based on secondary analyses of randomised trials in which 309
the main objective was not to study UI but instead the cardiovascular morbidity of HRT. So 310
the level of evidence contributed by these secondary analyses is lower. 311
Certain pathophysiological data would tend to indicate a worsening of UI due to lack of 312
œstrogen. However, in contradiction with this postulate, the epidemiological data obtained 313
with the cohorts shows that the menopause has little if any effect on urinary symptoms. The 314
results of several large randomised trials in the general population reveal an aggravation of UI 315
in case of systemic HRT. This detrimental effect of HRT needs to be seen in the light of what 316
is observed during pregnancy, when an increase in the prevalence of UI is observed [42]. This 317
greater prevalence of UI during pregnancy could be explained by the increase in œstrogen 318
concentrations. 319
Topical vaginal œstrogen therapy alone appears to have a beneficial effect on overactive 320
bladder symptoms. This effect could be explained by the improvement in terms of vaginal 321
dryness and a drop in recurrent urinary infections [8,11]. The learned societies do not 322
recommend the use of œstrogens (whether or not associated with progesterone) for the 323
treatment of UI. However, in case of overactive bladder symptoms in a post-menopausal 324
woman, topical vaginal treatment may be proposed [43,44]. 325
326
5. Conclusion 327
Female urinary incontinence is a complex and dynamic phenomenon, related with age and a 328
many other factors that can change with time. In order to gain greater insight, longitudinal 329
studies are necessary, with several years or even decades of follow-up in order to clarify its 330
evolution and risk factors. 331
The onset and/or worsening of UI at the menopause that is expected on the basis of 332
physiological observations is not confirmed by the results of most of the epidemiological 333
studies that mostly cover a large number of women followed up over many years. Moreover, 334
correction of the lack of œstrogen by HRT gives rise to paradoxical results that depend on the 335
type of UI and mode of administration. Systemic œstrogen therapy results in an increase in UI 336
12
symptoms and SUI in particular. Topical vaginal administration appears to be the most 337
beneficial by improving overactive bladder symptoms. 338
339
6. References 340
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